ReviewAging and disease2024
ROS-Induced Endothelial Dysfunction in the Pathogenesis of Atherosclerosis.
Review in Aging and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
57 citing papers in PubMed, 35 citations in OpenAlex.
- Antioxidants in Oxidative Stress and Obesity-Associated Diseases: Molecular Mechanisms and Potential Health Implications.Biomedicines · 2026Review
- Exercise in Patients with Subclinical Atherosclerosis: Mechanisms, Clinical Evidence, and Practical Recommendations.Current atherosclerosis reports · 2026Review
- Article
- Endothelial dysfunction: A central mechanism linking autosomal dominant polycystic kidney disease and intracranial aneurysms (Review).International journal of molecular medicine · 2026Review
- Mesoporous Silica-Confined Ruthenium Nanozyme Motors Reprogram Redox-Inflammatory Crosstalk to Suppress Atherosclerosis via NRF2 Nuclear Translocation.Advanced healthcare materials · 2026Article
- Article
- Ginkgo biloba L. in preventing cardiovascular disease: pharmacological effects, mechanism of action, and therapeutic potential.Acta pharmacologica Sinica · 2026Review
- Pulsatility as a Potential Regulator of Cardiovascular Biology: Molecular, Cellular, and Hemodynamic Remodeling During Continuous-Flow Left Ventricular Assist Device Support and Following Heart Transplantation.International journal of molecular sciences · 2026Review
- Metainflammation, Mitochondrial Dysfunction, and Organokine Crosstalk: A Central Axis Linking Metabolic Syndrome to Cardiovascular Diseases.International journal of molecular sciences · 2026Review
- A dual-mechanism injectable hydrogel integrating reactive oxygen species regulationand low-level laser therapy for androgenetic alopecia remediation.Journal of nanobiotechnology · 2026Article
- Causal Relationship between Dietary-Derived Antioxidants and Erectile Dysfunction: A Mendelian Randomization Study.The world journal of men's health · 2026Article
- Mitochondrial UQCRC2 as a Redox-Regulatory Node in Metabolic and Cardiometabolic Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Research Progress on the Molecular Mechanism of LRP1 and TGFβ-PDGFRβ Signaling Network in Atherosclerosis and Vascular Remodeling.International journal of molecular sciences · 2026Review
- Simulated microgravity induces a NOX-sensitive oxidative response that is attenuated by resveratrol in human endothelial cells.Scientific reports · 2026Article
- Hesperetin-7-O-Glucuronide Improves Endothelial Cell Function Through Improving NO/ET-1 Balance and Reducing Oxidative Stress via miRNAs.Current issues in molecular biology · 2026Article
- Composite dietary antioxidant index and risk of metabolic dysfunction - associated steatotic liver disease: evidence from a prospective cohort study.Nutrition & metabolism · 2026Article
- The Role of Cytokines in Vascular Endothelial Glycocalyx Integrity and Impairment Following Open-Heart Surgery.Biomedicines · 2026Review
- The Role of Long Non-Coding RNA in Atherosclerosis: Mechanism and Intervention of Traditional Chinese Medicine.International journal of molecular sciences · 2026Review
- Oscillatory shear stress-driven endothelial-to-mesenchymal transition: a critical mechanical signal transduction mechanism in atherosclerosis progression.Cell death discovery · 2026Review
- Inflammaging and Cardiovascular Risk in Old Women.High blood pressure & cardiovascular prevention : the official journal of the Italian Society of Hypertension · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Various signaling pathways are regulated by reactive oxygen species (ROS), which are radical oxygen intermediates under normal physiological conditions. However, when the buffering capacity of antioxidant enzymes is exceeded by the accumulation of ROS, oxidative stress, and endothelial cell dysfunction occur, which have been recognized as key contributors to the development of atherosclerosis. In this review, an overview is provided on mechanisms underlying ROS generation in endothelial cells and the involved regulatory pathways. Further, we discuss the ROS induced endothelial cell dysfunction and its relationship with atherosclerosis. Current knowledge on ROS-induced endothelial impairment is presented, characterized by decreased NO bioavailability, intracellular dysfunction and ox-LDL accumulation. Furthermore, biomarkers such as oxidative products of lipid, protein, and nucleotide are discussed as measurements for ROS levels. Novel interventions targeting oxidative stress are listed as potential pharmacotherapies in clinical practice. In conclusion, this review presents a systematic analysis of the mechanisms underlying ROS generation and elucidates how manipulation of these mechanisms can safeguard endothelial cell function.
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.